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We assessed a kallikrein-like amidase activity probably related to the kallikrein-kinin system, as well as the participation of leukocyte infiltration in renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min of ischemia and to different periods of reperfusion. A control group consisted of sham-operated mice, under similar conditions, except for ischemia induction. Kallikrein-like amidase activity, Evans blue extravasation and myeloperoxidase activity were measured in kidney homogenates, previously perfused with 0.9 percent NaCl. Plasma creatinine concentration increased only in the 60-min ischemic group. After 20 min of ischemia and 1 or 24 h of reperfusion, no change in kallikrein-like amidase activity or Evans blue extravasation was observed. In the mice subjected to 20 min of ischemia, edema was evident at 1 h of reperfusion, but kidney water content returned to basal levels after 24 h of reperfusion. In the 60-min ischemic group, kallikrein-like amidase activity and Evans blue extravasation showed a similar significant increase along reperfusion time. Kallikrein-like amidase activity increased from 4 nmol PNA mg protein-1 min-1 in the basal condition to 15 nmol PNA mg protein-1 min-1 at 10 h of reperfusion. For dye extravasation the concentration measured was near 200 µg of Evans blue/g dry tissue in the basal condition and 1750 µg of Evans blue/g dry tissue at 10 h of reperfusion. No variation could be detected in the control group. A significant increase from 5 to 40 units of DAbs 655 nm g wet tissue-1 min-1 in the activity of the enzyme myeloperoxidase was observed in the 60-min ischemic group, when it was evaluated after 24 h of reperfusion. Histological analysis of the kidneys showed migration of polymorphonuclear leukocytes from the vascular bed to the interstitial tissue in the 60-min ischemic group after 24 h of reperfusion. We conclude that the duration of ischemia is critical for the development of damage during reperfusion and that the increase in renal cortex kallikrein-like amidase activity probably released from both the kidney and leukocytes may be responsible, at least in part, for the observed effects, probably through direct induction of increased vascular permeability.

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We assessed a kallikrein-like amidase activity probably related to the kallikrein-kinin system, as well as the participation of leukocyte infiltration in renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min of ischemia and to different periods of reperfusion. A control group consisted of sham-operated mice, under similar conditions, except for ischemia induction. Kallikrein-like amidase activity, Evans blue extravasation and myeloperoxidase activity were measured in kidney homogenates, previously perfused with 0.9% NaCl. Plasma creatinine concentration increased only in the 60-min ischemic group. After 20 min of ischemia and 1 or 24 h of reperfusion, no change in kallikrein-like amidase activity or Evans blue extravasation was observed. In the mice subjected to 20 min of ischemia, edema was evident at 1 h of reperfusion, but kidney water content returned to basal levels after 24 h of reperfusion. In the 60-min ischemic group, kallikrein-like amidase activity and Evans blue extravasation showed a similar significant increase along reperfusion time. Kallikrein-like amidase activity increased from 4 nmol PNA mg protein-1 min-1 in the basal condition to 15 nmol PNA mg protein-1 min-1 at 10 h of reperfusion. For dye extravasation the concentration measured was near 200 microg of Evans blue/g dry tissue in the basal condition and 1750 microg of Evans blue/g dry tissue at 10 h of reperfusion. No variation could be detected in the control group. A significant increase from 5 to 40 units of DeltaAbs 655 nm g wet tissue-1 min-1 in the activity of the enzyme myeloperoxidase was observed in the 60-min ischemic group, when it was evaluated after 24 h of reperfusion. Histological analysis of the kidneys showed migration of polymorphonuclear leukocytes from the vascular bed to the interstitial tissue in the 60-min ischemic group after 24 h of reperfusion. We conclude that the duration of ischemia is critical for the development of damage during reperfusion and that the increase in renal cortex kallikrein-like amidase activity probably released from both the kidney and leukocytes may be responsible, at least in part, for the observed effects, probably through direct induction of increased vascular permeability.

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The purpose of the present work was to evaluate the kallikrein-kinin system and effects of hypothermia during renal ischemia and reperfusion. Male C57BL/KSJmdb mice were subjected to 20 or 60 min ischemia for different periods of reperfusion. Our results demonstrate that short periods of ischemia followed by reperfusion did not cause significant alterations in kallikrein activity, Evans Blue (EB) extravasation, prokallikreins, myeloperoxidase activity or plasma creatinine concentration. Edema was evident at 1 h reperfusion in the treated mice, but returned to basal values after 24 h reperfusion. Kallikrein activities and EB extravasation showed a significant increase in 60 min ischemic mice. Myeloperoxidase activity in the kidney of the mice confirmed net infiltration in the group with 60 min ischemia and 24 h reperfusion. The generation of kinins and activation of matrix degrading enzymes by tissue kallikrein, liberated from both renal and infiltrated leukocytes, could be responsible at least in part for the damage observed in the kidney of mice subject to 60 min ischemia and reperfusion. The hypothermia significantly reduced the inflammatory process in the 60 min ischemic mice, and did prevent an increase in vascular permeability. Nevertheless, the tissue edema was not shown to change between normothermic and hypothermic ischemic mice.

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Islet inflammation or insulitis is followed by selective destruction of the insulin secreting B-cell. Animal models of insulin-dependent diabetes mellitus (IDDM) have been used to characterize more fully insulitis, and our results with C57/BL/Ks mdb with low doses of streptozotocin (STZ) confirmed the disease. B1 receptor antagonist [Leu8]des-Arg9-BK has shown a significant effect on diabetic glycemia and renal control parameters. Compared to insulin, the drug was effective to prevent the insulitis and the renal damage. On the other hand, B2 receptor antagonist (HOE 140) and ACE-I (captopril) were only able to control the urinary diabetic proteinuria.

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La toxicidad renal por ifosfamida puede ser potenciada por otras drogas. Se reporta un paciente varón de 57 años de edad con carcinoma indiferenciado de pulmón no a celulas pequeñas, estadio IIIB. Recibió cada 28 días ifosfamida 2,5 g/m2, días 1 y 15, dexametasona 8 mg, MESNA 4,8 g/ciclo y clorhidrato de granisetrón. Con orina y función renal normales, se realizó TAC de tórax con contraste y a las tres semanas recibió un cuarto ciclo. Un mes despues ingresó con IRA no oligúrica, urea 306 mg/dl, CrP 11 mg/dl, Kp 3 meq, Nap 130 mq/, Na urinario 30.5 meq/l, Hb 9,6 g/dl, GB 11.000, hipergamma con componente M gamma lento Kappa y Lambda, proteinuria 1.2 g/24 horas, tubular, Bence Jones negativa y microhematuria. Ecografía renal normal. La PAMO descartó plasmocitoma. La biopsia renal mostró nefritis túbulo - intersticial con necrosis y atrofia tubular, fibrosis instersticial y afectación glomerular con proliferación celular e inmunofluorescencia negativa. Realizó tratamiento medico con recuperación parcial de la función renal y proteinuria negativa a los seis meses. Se recomienda no utilizar contrastes iodados durante el tratamiento con ifosfamida y monitorear beta 2 microglobulina y función renal como indicadores de daño renal

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La toxicidad renal por ifosfamida puede ser potenciada por otras drogas. Se reporta un paciente varón de 57 años de edad con carcinoma indiferenciado de pulmón no a celulas pequeñas, estadio IIIB. Recibió cada 28 días ifosfamida 2,5 g/m2, días 1 y 15, dexametasona 8 mg, MESNA 4,8 g/ciclo y clorhidrato de granisetrón. Con orina y función renal normales, se realizó TAC de tórax con contraste y a las tres semanas recibió un cuarto ciclo. Un mes despues ingresó con IRA no oligúrica, urea 306 mg/dl, CrP 11 mg/dl, Kp 3 meq, Nap 130 mq/, Na urinario 30.5 meq/l, Hb 9,6 g/dl, GB 11.000, hipergamma con componente M gamma lento Kappa y Lambda, proteinuria 1.2 g/24 horas, tubular, Bence Jones negativa y microhematuria. Ecografía renal normal. La PAMO descartó plasmocitoma. La biopsia renal mostró nefritis túbulo - intersticial con necrosis y atrofia tubular, fibrosis instersticial y afectación glomerular con proliferación celular e inmunofluorescencia negativa. Realizó tratamiento medico con recuperación parcial de la función renal y proteinuria negativa a los seis meses. Se recomienda no utilizar contrastes iodados durante el tratamiento con ifosfamida y monitorear beta 2 microglobulina y función renal como indicadores de daño renal (AU)

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Sub-diabetogenic doses of streptozotocin (STZ) produce insulitis, beta cell destruction and diabetes in mice. Since kinin have been proposed as an inflammatory mediator in several diseases, we decided to evaluate the role of the kallikrein-kinin system in the evolution of insulitis. Male C 57 BL/KsJ mdb mice were injected with STZ (40 mg/kg) for 5 consecutive d. Aprotinin (4000 KIU/d) was injected simultaneously with STZ during 10 d. Plasma and urine samples collected on day 15 were assayed for glucose concentration and proteins, nitrites and kallikrein. Diabetic mice showed hyperglycemia and increased diuresis, marked proteinuria, nitrites and kallikrein. Administration of aprotinin, a potent tissue kallikrein inhibitor, to STZ mice, reduced the hyperglycemia and the altered renal function of the diabetic mice to level no different from normal mice. The present studies are consistent with the hypothesis that the over-production of tissue kallikrein in insulitis could be controlled by the effect of aprotinin.

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The resistance to changes in the osmolarity of boar sperm was used to measure the resistance of boar sperm cells against freezing/thawing. Semen was incubated for 5 min in different solutions ranging from about 600 mOsm to about mOsm, and at 4 degrees C, 16 degrees C or 37 degrees C (undisturbed media). This undisturbed media was constituted by NaCl, glycerol or glucose. This semen was then placed in an isoosmotic solution (disrupted solutions). Incubation in undisturbed media did not alter the percentages of viability or altered acrosomes, except when the initial incubation has been at 37 degrees C and with osmolarities above 1000 mOsm. Viability and altered acrosome statistics were strongly modified in disrupted media. These effects are dependent upon the initial osmolarity of the media, but not upon the temperature. Pre-incubation with ouabain or amiloride did not affect spermatozoa incubated at 16 degrees C in a 2211 mOsm, NaCl medium. However, in sperm incubated in this 2211 mOsm medium and then rapidly placed in an isoosmotic solution, ouabain induced a decrease in viability and an increase in altered acrosomes. Amiloride did not affect the response of cells to the disrupted medium. Some significant correlations were observed among the percentages of altered acrosomes after hyperosmotic stress and some quality parameters of the fresh boar semen, especially the motion parameters. Although the resistance to hyperosmotic stress could be a valuable parameter in assessing fresh quality analysis, its usefulness in frozen-thawed semen is compromised, since other factors beside osmotic changes are involved in the resistance of boar semen to freezing-thawing. The NA+/K+, ouabain-dependent ATP-ase activity seems to be related to the mechanisms of resistance to hyperosmotic stress in boar sperm.

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Although hypoosmotic tests are widely used to assess spermatozoal quality in different species, they have not been used extensively in the stallion. Moreover, the role of the Na (+)K (+), ouabain sensitive-ATP-ase in the response of equine sperm to hypoosmotic shock is not well understood. This study tests two hypotheses: 1) that equine spermatozoa will respond to a hypoosmotic medium by swelling of the tail, and 2) that addition of ouabain will increase the percentage of swollen sperm tails. Ejaculates from 3 stallions were collected with an artificial vagina and diluted in Kenney's medium (Time = 0). Aliquots were randomly selected to be incubated in an isoosmotic (297 mOsm) or different hypoosmotic media that were composed of citrate or of citrate wïth fructose. The osmolarity of the hypoosmotic media with citrate ranged from 18 to 96 mOsm, and the medium composed of citrate plus fructose (HOS medium) was of 153 mOsm. Moreover, aliquots of spermatozoa pretreated with ouabain were added to the isoosmotic medium and also to the HOS and the 96 mOsm citrate medium (ORT medium). Incubation of equine sperm in the hypoosmotic media resulted in a time- and osmolarity-dependent swelling of the sperm tail, reaching maximum values after incubation for 20-30 min in both the HOS and ORT media. Ouabain induced a dose-dependent effect on swollen tails and viability in fresh semen and also affected some parameters related to motility. Ouabain also increased the swelling response in a hypoosmotic medium although viability decreased. The percentage of swollen tails after incubation in ORT and HOS media snowed significant correlations to viability, altered acrosomes and total motility, but not to other parameters of horse semen analysis. Our results suggest that hypoosmotic tests could be used to improve standard horse semen analysis. Additionally, Na (+)K (+)-ATP-ase activity could be related to the response against hypoosmotic shock of horse spermatozoa.

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To study the resistance of horse spermatozoa against hyperosmotic stress, cells were incubated in solutions of 600 to 4000 mOsm(undisturbed media). Then, semen was immediately placed into an iso-osmotic solution (disrupted media). Incubation in undisturbed media decreased sperm viability in an osmolarity- and temperature-dependent manner. Viability was further decreased in disrupted media, with the effect dependent upon the initial osmolarity of the media and on the temperature. Treatment with ouabain or amiloride impaired the resistance of horse spermatozoa to hyperosmotic stress. Very few correlations were strong between viability after hyperosomotic stress and quality parameters of fresh and frozen-thawed horse semen. The results indicate that the usefulness of resistance to hyperosmotic stress in assessing frozen-thawed semen quality is compromised, since other factors are involved in the resistance to freezing-thawing. Both Na (+)K (+) ATP-ase and the Na (+)H (+) antiporter act in the resistance to hyperosmotic stress in horse spermatozoa.

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The recently described monocytoid B-cell lymphoma is a low-grade lymphoma presenting most frequently in elderly women and commonly associated with autoimmune diseases. Leukaemic expression of this disease has been reported in advanced stages. A case of monocytoid lymphocytosis without lymph node enlargement is presented herein. A 60-year old woman complaining of easy bruises was found to have a 2-cm splenomegaly. Her laboratory data included the following: haemoglobin, 125 g/L; haematocrit, 0.35 L/L; white cell count, 29 x 10(9)/L with 32% PMN, 3% stabs, 2% myelocytes, 1% metamyelocytes, 30% lymphocytes and 32% atypical mononucleated cells showing wide, pale cytoplasm neatly contoured and oval nucleus with monocytoid features. The basal coagulation study showed prothrombin 50%, APTT 40 seconds, fibrinogen 68 mg/dL and FDP between 80 and 160 ng/dL. Splenomegaly without lymph-node enlargement was found on CT scan. The bone-marrow biopsy showed a 68% monocytoid lymphocytic infiltration, acid-phosphatase positive and tartrate-sensitive, without fibrosis. Bone-marrow and peripheral immunophenotype showed those cells to be CD22, CD 19 and CD11 positive, while T and CD25 markers were absent. The patient was treated with alpha-2b interferon at a dose of 3MU three times a week for 6 months, with general improvement and regression of the leukaemic expression. Eleven months after diagnosis she died of a central nervous system haemorrhage. The morphological, immunological and cytochemical features of the monocytoid lymphocytes in this case are commented, along with their variable behaviour. A review of the literature is also carried out, attention being laid on the onset and the response to therapy of B-cell monocytoid lymphomas as the singularity of this case lies on its exclusively leukaemic onset. It is concluded that an interrelationship between monocytoid B-lymphocytic leukaemia and B-cell monocytoid lymphoma might possibly exist, such as that between chronic lymphocytic leukaemia and diffuse lymphocytic lymphoma.

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We investigated the relationship between the level of c-myc mRNA and histologic aggressiveness in thyroid tumors obtained at surgery. In thyroid carcinomas, there was a positive correlation between these two parameters, while in benign tumors there was no correlation between cellularity and the expression of the proto-oncogene c-myc. These results might be useful in the prognosis of thyroid tumors and consequently helpful in the management of the patient.

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We report 72 years old woman, with adenoacamthoma of the upper osophagus who was admitted in Hospital israelita "EZRAH" in April of 1991. We performed a review of the literature on this rare tumour, that is the reason of presenting this case

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We report 72 years old woman, with adenoacamthoma of the upper osophagus who was admitted in Hospital israelita "EZRAH" in April of 1991. We performed a review of the literature on this rare tumour, that is the reason of presenting this case (AU)

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We report a 72 year-old woman, with adenoacanthoma of the upper esophagus who was admitted in Hospital Israelita "EZRAH" in April of 1991. We performed a review of the literature on this rare tumour, that is the reason of presenting this case.

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We report a 72 year-old woman, with adenoacanthoma of the upper esophagus who was admitted in Hospital Israelita [quot ]EZRAH[quot ] in April of 1991. We performed a review of the literature on this rare tumour, that is the reason of presenting this case.

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We report a 72 year-old woman, with adenoacanthoma of the upper esophagus who was admitted in Hospital Israelita [quot ]EZRAH[quot ] in April of 1991. We performed a review of the literature on this rare tumour, that is the reason of presenting this case.

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